AB0565 PREVALENCE OF LIVER FIBROSIS ASSESSED BY TRANSIENT ELASTOGRAPHY IN PATIENTS WITH SJÖGREN’S SYNDROME
Authors: T. Androutsakos, T. Voulgaris, A. D. Bakasis, M. L. Koutsompina, L. Chatzis, O. Argyropoulou, V. Pezoulas, D. I. Fotiadis, A. Goules, G. Papatheodoridis, A. Tzioufas
Journal: Annals of the Rheumatic Diseases (2022)

Background Liver is considered one of the most commonly involved extra-glandular organs in patients with Sjögren’s syndrome (SS). Primary biliary cholangitis, hepatitis C virus infection, non-alcoholic fatty liver disease (NAFLD) and drug hepatotoxicity are the major contributors of liver disease among SS patients. Especially, NAFLD comprises a major health problem worldwide with a rapidly rising incidence and a prevalence of approximately 25% in the general population. In both NAFLD and SS, inflammatory and apoptotic pathways are implicated in pathogenesis, pathways that are also linked to fibrogenesis. No studies so far have investigated the net effect of SS in liver fibrosis. Objectives To assess whether SS is associated with advanced liver fibrosis (LF) in the absence of viral, alcohol-related, autoimmune hepatitis or primary cholangitis. Methods In this prospective study, consecutive SS patients from the rheumatology outpatient clinic of the Department of Pathophysiology, “Laiko” General Hospital, Athens, Greece between June 1 st and December 31 st , 2021, underwent transient elastography (TE) with measurement of liver stiffness and controlled attenuation parameter, assessing LF and liver steatosis (LS), respectively. For LF the following cut-offs were used: F0-1: 2-7 kPa, F2: 7-10 kPa, F3: 10-14 kPa, and F4: &gt;14 kPa. F0-F1 stages were considered as clinically insignificant and F2-F4 as advanced. For LS the following cut-offs were used: S0-S1: 100-260 dB/m, S2: 260-290 dB/m, and S3: &gt;290 dB/m. LS stage S0-S1 was classified as low and S2-S3 as high. Individuals who were evaluated in the hepatology outpatient clinic for possible NAFLD/LS based on ultrasonographic criteria (higher echogenicity than renal cortex and/or splenic parenchyma) served as a comparator group. In all participants, those with viral or alcoholic hepatitis, autoimmune liver diseases, transaminasemia or liver disease attributed to drug hepatotoxicity were excluded. Clinical, demographic and laboratory data were collected from all participants at the time of TE. Results Fifty-two patients with SS (49 females, 94.2%) with a median disease duration (range) of 8 (1-46) years and 198 comparators (104 females, 52.5%) were included in this study. The median age (range) of SS and comparators was 62.5 (30-81) and 55 (19-86) years, respectively. Comparators and SS patients had comparable prevalence regarding type 2 diabetes mellitus (T2DM), hyperlipidemia and body-mass index (BMI). Patients with SS had less frequently high LS (27% vs 62%, p&lt;0.001) and advanced LF [2 (3.8%) vs 34 (17.2%), p=0.014], compared to comparator group. The 2 SS patients with advanced LF had also high LS. Univariable analysis in terms of T2DM, hyperlipidemia, BMI, age, gender, steatosis, and disease status (SS or comparators) between individuals with insignificant and advanced LF revealed age, liver steatosis, BMI, and disease status as the only statistically significant parameters; of these, only age was finally identified as independent risk factor in the multivariable logistic regression analysis (Table 1). Table 1. Multivariable logistic regression analysis for risk factors associated with advanced liver fibrosis among patients with Sjögren’s Syndrome and comparators. Variables Coefficient Odds ratio p-value CI low CI upper Age 0.057 1.059 0.023 1.019 1.1 Body Mass Index 0.099 1.105 0.121 1.012 1.207 Presence of Sjögren’s syndrome -0.941 0.419 0.346 0.067 2.826 High Liver Steatosis 0.344 1.473 0.62 0.355 6.167 Conclusion Sjögren’s syndrome per se is not associated with advanced liver fibrosis. References [1]Kaplan, M.J., et al. The liver is a common non-exocrine target in primary Sjögren’s syndrome: a retrospective review. BMC Gastroenterol 2002 , 2 , 21, doi:10.1186/1471-230x-2-21. [2]Montaño-Loza, A.J., et al. Abnormal hepatic biochemistries and clinical liver disease in patients with primary Sjögren’s syndrome. Ann Hepatol 2007 , 6 , 150-155. Disclosure of Interests None declared